Cutting Edge: CNS CD11c+ Cells from Mice with Encephalomyelitis Polarize Th17 cells and Support CD25+CD4+ T cell-Mediated Immunosuppression, Suggesting Dual Roles in the Disease Process
Author(s) -
Pratima Deshpande,
Irah L. King,
Benjamin M. Segal
Publication year - 2007
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.178.11.6695
Subject(s) - experimental autoimmune encephalomyelitis , immunology , il 2 receptor , immunosuppression , cd11c , t cell , haematopoiesis , encephalomyelitis , biology , immune system , medicine , multiple sclerosis , microbiology and biotechnology , stem cell , phenotype , biochemistry , gene
CD11c(+) dendritic cells (DCs) are a prominent component of CNS infiltrates in mice with experimental autoimmune encephalomyelitis. However, their role in immunopathogenesis is controversial. In this study, we report that they originate from peripheral hemopoietic cells and exhibit diverse functions that change during the course of acute disease. CNS DCs stimulate naive T cells to proliferate and polarize Th(17) responses when harvested shortly following disease onset but are relatively inefficient APC by the time of peak disability. Conversely, they can support CD4(+)CD25(+) T cell-mediated immunosuppression early during experimental autoimmune encephalomyelitis. Such paradoxical functions might reflect dual roles of CNS DCs in promoting local inflammation while setting the stage for remission.
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